The visualization of chromosomal aneuploidy and copy number changes of specific cancer-associated genes has become an important complement to routine morphological assessment of cytological samples.1 This approach is biologically valid and successful because chromosomal aneuploidy and the resulting genomic imbalances are specific for cancer cells, distinct for different carcinomas, and occur early during disease progression.2,3 Some genomic imbalances are correlated with poor prognosis and treatment failure,4-6 and others, such as amplification of the Her2/neu oncogene in breast cancer, can guide therapeutic decisions.7 
Like most other human carcinomas, cervical cancers are defined by a conserved distribution of genomic imbalances. In addition to infection with high-risk human papilloma virus,9,10 the sequential transformation of cervical squamous epithelium requires the acquisition of additional copies of chromosome arm 3q,11 among other cytogenetic abnormalities.12 CGH analyses of cervical carcinomas have shown that more than 85% of invasive cervical carcinomas carry specific genomic imbalances that result in copy number increases of chromosome arm 3q.5,11,20-26 The region of minimal overlap points to chromosome band 3q26, which contains the gene for the RNA component of human telomerase (TERC).27 
The implementation of cervical cancer screening programs has greatly reduced disease incidence and mortality in industrialized countries.16,17 However, a single cytological evaluation remains relatively insensitive, hence the need for frequent follow-up investigations. This is attributable to sampling or interpretation errors, and to the fact that some early lesions may not have acquired recognizable phenotypic alterations.17 Invasive cervical carcinomas develop through increasing stages of cervical dysplasia and advance to CIN3, which is considered a bonafide precancerous lesion that requires surgical intervention. However, only about 10-15% of all low-grade dysplastic lesions follow this path of linear progression. The identification of markers of disease progression would therefore be of great clinical interest.
A previous study demonstrated that visualization of additional copies of TERC can serve as a specific and sensitive test for 3q26 amplification in routinely collected cytological samples, including samples of low grade cervical dysplasia.8 This finding was consistent with, but not conclusive of, the hypothesis that the 3q-imposed growth advantage reflects a point of no return during the sequential malignant transformation of cervical epithelial cells. For example, U.S. application Ser. No. 10/857,859, filed on Jun. 4, 2004 and published as U.S. Application Publication No. 20050026190, indicates that the 3q26 amplification can be used to selectively detect high grade cervical intraepithelial neoplasias (CIN II and CIN III) and malignant carcinomas in cervical biopsy and pap smear specimens without detecting low grade cervical intraepithelial neoplasia. Thus, the 3q26 amplification was thought to be a distinguishing factor between low grade and high grade cervical dysplasias and adenocarcinomas.